Epigenetic Programming of the mouse germ line. (360G-Wellcome-075542_Z_04_A)

Epigenetic Programming of the mouse germ line Major epigenetic reprogramming of the germ line occurs in the primodial germ cells (PGCs) in which parental imprints are erased. This is brought about by the dynamic removal and re-establishment of epigenetic marks in the nucleus, essentially involving histone modifications, DNA (de)methylation and chromatin remodelling. Both arginine and lysine residues can be methylated and one of the ways these histone modifications transmit their biological signals is through local binding factors (effector proteins) that recognise the distinct methylation marks. Currently, little is known about the identity of effectors that recognise methyl-arginine modifications. Very recently, tudor-domain containing proteins were shown to be able to bind to symmetric methylated arginines in polypeptides and were postulated to be general methyl-binding proteins. These are strong candidates that may be general effectors of methylarginine on histone tails. I will examine if this putative histone methyl-binding capability exists, and if so, how tudor proteins may potentially contribute to the germ line chromatin state during epigenetic reprogramming. Notably, my preliminary data have shown that several of these tudor-domain containing proteins appear to be restricted to the germ line, and absent in the soma. This strongly suggests that tudor family of proteins may have uncharacterised functions in germ line development in addition to a putative methyl-arginine binding ability. Although it remains to be established if tudor proteins are methylarginine effectors, their potential involvements in germ line development are interesting in their own rights. Finally, I am also aware of the possible wider roles of tudor proteins in pluripotency, and will address this possibility.